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The Oxford Handbook of the Ends of Empire
The Oxford Handbook of the Ends of Empire offers the most comprehensive treatment of the causes, course, and consequences of the ends of empire in the twentieth century. The volume's contributors convey the global reach of decolonization, with chapters analysing the empires of Western Europe, Eastern Europe, China and Japan. The Handbook combines broad, regional treatments of decolonization with chapter contributions constructed around particular themes or social issues. It considers how the history of decolonization is being rethought as a result of the rise of the 'new' imperial history, and its emphasis on race, gender, and culture, as well as the more recent growth of interest in histories of globalization, transnational history, and histories of migration and diaspora, humanitarianism and development,0and human rights. The Handbook, in other words, seeks to identify the processes and commonalities of experience that make decolonization a unique historical phenomenon with a lasting resonance. In light of decades of historical and social scientific scholarship on modernization, dependency, neo-colonialism, 'failed state' architectures and post-colonial conflict, the obvious question that begs itself is 'when did empires actually end?' In seeking to unravel this most basic dilemma the Handbook explores the relationship between the study of decolonization and the study of globalization. It connects histories of the late-colonial and post-colonial worlds, and considers the legacies of empire in European and formerly colonised societies.
Book
Circulating giant macrophages as a potential biomarker of solid tumors
Tumor-associated macrophages (TAMs) derived from primary tumors are believed to facilitate circulating tumor cell (CTC) seeding of distant metastases, but the mechanisms of these processes are poorly understood. Although many studies have focused on the migration of CTCs, less attention has been given to TAMs that, like CTCs, derive from tumor sites. Using precision microfilters under low-flow conditions, we isolated circulating cancer-associated macrophage-like cells (CAMLs) from the peripheral blood of patients with breast, pancreatic, or prostate cancer. CAMLs, which are not found in healthy individuals, were found to express epithelial, monocytic, and endothelial protein markers and were observed bound to CTCs in circulation. These data support the hypothesis that disseminated TAMs can be used as a biomarker of advanced disease and suggest that they have a participatory role in tumor cell migration.
Journal Article
Detyrosinated microtubules modulate mechanotransduction in heart and skeletal muscle
In striated muscle, X-ROS is the mechanotransduction pathway by which mechanical stress transduced by the microtubule network elicits reactive oxygen species. X-ROS tunes Ca
2+
signalling in healthy muscle, but in diseases such as Duchenne muscular dystrophy (DMD), microtubule alterations drive elevated X-ROS, disrupting Ca
2+
homeostasis and impairing function. Here we show that detyrosination, a post-translational modification of α-tubulin, influences X-ROS signalling, contraction speed and cytoskeletal mechanics. In the
mdx
mouse model of DMD, the pharmacological reduction of detyrosination
in vitro
ablates aberrant X-ROS and Ca
2+
signalling, and
in vivo
it protects against hallmarks of DMD, including workload-induced arrhythmias and contraction-induced injury in skeletal muscle. We conclude that detyrosinated microtubules increase cytoskeletal stiffness and mechanotransduction in striated muscle and that targeting this post-translational modification may have broad therapeutic potential in muscular dystrophies.
Microtubules are transducers of mechanical energy in muscle cells. Here, the authors show that mechanotransduction is regulated by post-translational detyrosination of microtubules in mouse heart and skeletal muscle, and that reducing detyrosination ameliorates symptoms in a model of Duchenne muscular dystrophy.
Journal Article
Insights on CTC Biology and Clinical Impact Emerging from Advances in Capture Technology
Circulating tumor cells (CTCs) and circulating tumor microemboli (CTM) have been shown to correlate negatively with patient survival. Actual CTC counts before and after treatment can be used to aid in the prognosis of patient outcomes. The presence of circulating tumor materials (CTMat) can advertise the presence of metastasis before clinical presentation, enabling the early detection of relapse. Importantly, emerging evidence is indicating that cancer treatments can actually increase the incidence of CTCs and metastasis in pre-clinical models. Subsequently, the study of CTCs, their biology and function are of vital importance. Emerging technologies for the capture of CTC/CTMs and CTMat are elucidating vitally important biological and functional information that can lead to important alterations in how therapies are administered. This paves the way for the development of a \"liquid biopsy\" where treatment decisions can be informed by information gleaned from tumor cells and tumor cell debris in the blood.
Journal Article
The rough guide to China
This guide to China enables you to explore the sights and attractions of the country, offers advice on where to stay and eat, and comments on China's history, politics, environment, and people.
Book
Polarized NHE1 and SWELL1 regulate migration direction, efficiency and metastasis
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. Here the authors show that the chloride ion channel SWELL1 and the ion exchanger NHE1 are preferentially enriched at the trailing and leading edges, respectively, of migrating cells and regulate cell volume to propel confined cells, favouring breast cancer cell extravasation and metastasis.
Journal Article
Superman Blue
\"When the sun temporarily goes out, the classic Superman as we know him temporarily loses his powers...but when they return, they are not at all what the Man of Steel expects! Clark Kent is suddenly transformed into a being of crackling blue energy, complete with a new set of abilities and a totally different look! But that's not where the story ends... The villainous Cyborg Superman and Toyman split the Man of Steel into two beings, Superman Red and Superman Blue! So who is the real Clark Kent? And will Metropolis now have two protectors?\"-- Provided by publisher.
Book
Distinct roles of tumor associated mutations in collective cell migration
Recent evidence suggests that groups of cells are more likely to form clinically dangerous metastatic tumors, emphasizing the importance of understanding mechanisms underlying collective behavior. The emergent collective behavior of migrating cell sheets in vitro has been shown to be disrupted in tumorigenic cells but the connection between this behavior and in vivo tumorigenicity remains unclear. We use particle image velocimetry to measure a multidimensional migration phenotype for genetically defined human breast epithelial cell lines that range in their in vivo behavior from non-tumorigenic to aggressively metastatic. By using cells with controlled mutations, we show that PTEN deletion enhances collective migration, while Ras activation suppresses it, even when combined with PTEN deletion. These opposing effects on collective migration of two mutations that are frequently found in patient tumors could be exploited in the development of novel treatments for metastatic disease. Our methods are based on label-free phase contrast imaging, and thus could easily be applied to patient tumor cells. The short time scales of our approach do not require potentially selective growth, and thus in combination with label-free imaging would allow multidimensional collective migration phenotypes to be utilized in clinical assessments of metastatic potential.
Journal Article